In: Nursing
myocardial infraction pathophysiology
MYOCARDIAL INFARCTION also called as 'Heart Attack', is the death of cardiac (heart) muscle due to prolonged severe ischemia ( ischemia means inadequate blood supply to a tissue causing death of the tissue).
PATHOPHYSIOLOGY OF MYOCARDIAL INFARCTION:
Myocardial infarction occurs due to coronary artery occlusion. Coronary artery supply blood to heart. An occlusion in these arteries results in ischemia of heart muscles and hence Myocardial infarction.
The sequence of pathophysiological events that underlie myocardial infarction are as follows:
• A coronary artery atheromatous plaque ( is an abnormal accumulation of material including fat, cholesteroal, calcium deposits in inner wall of coronary artery) undergoes an acute change consisting of intraplaque hemorrhage, erosion or ulceration, or rupture or fissuring.
• When exposed to subendothelial collagen and necrotic plaque contents, platelets adhere , become activated , release their granule contents, and aggregate to form microthrombi.
• Vasospasm is stimulated by mediators released from platelets.
• Tissue factor activates the coagulation pathway, adding to the bulk of the thrombus.
• Within minutes, the thrombus can expand to completely occlude the vessel lumen.
After the complete occlusion of coronary vessel, the blood supply to heart is compromised which leads to ischemia of heart muscles resulting in myocardial infarction.
In approximately 10% cases, transmural Myocardial infarction occurs in absence of the typical coronary atherothrombosis . In such cases other mechanisms are responsible for reduced coronary blood flow, including:
• VASOSPASM with or without coronary atherosclerosis, perhaps in association with platelet aggregation or due to drug ingestion (example cocaine or ephedrine).
• Emboli from the left atrium in association with atrial fibrillation, a left sided mural thrombus , vegetations of infective endocarditis , intracardiac prosthetic material, or paradoxical emboli from the right side of the heart or the peripheral veins , traversing a patent foramen ovale and into the coronary arteries.
• Ischemia without detectable or significant coronary atherosclerosis and thrombosis may be caused by disorders of small intramural coronary vessels (example vasculitis ), hematologic abnormalities (example sickle cell disease), amyloid deposition in vascular walls, vascular dissection, marked hypertrophy (example aortic stenosis), lowered systemic blood pressure (example shock), or inadequate myocardial protection during cardiac surgery.
Coronary arterial obstruction diminishes blood flow to a region of myocardium causing ischemia, rapid myocardial dysfunction and eventually with prolonged vascular compromise cause myocyte death. The anatomic region supplied by that artery is referred to as the area at risk. The outcome depends predominantly on the severity and duration of flow deprivation.